A patient with a known bee venom allergy is stung a second time and develops systemic anaphylaxis within minutes. Which mechanism explains this response?
AIgG antibodies from prior exposure attack mast cells in blood vessel walls, activating complement
BIgE antibodies already bound to mast cells are crosslinked by venom proteins, triggering rapid degranulation of preformed mediators
CSoluble antigen-antibody complexes deposit in the skin and recruit neutrophils
DMemory T cells from the first sting migrate to the site over 24–72 hours and release cytokines
This is Type I (immediate) hypersensitivity. The first sting primed mast cells by inducing IgE production; IgE bound to FcεRI receptors on mast cells. Re-exposure crosslinks adjacent IgE molecules, triggering explosive degranulation within minutes — releasing histamine and other preformed mediators. The speed is diagnostic: preformed mediators are immediately available. Type IV (T cells) takes 24–72 hours, ruling out option D. Type III involves immune complex deposition, not mast cell degranulation.
Question 2 Multiple Choice
Weeks after a streptococcal throat infection, a patient develops glomerulonephritis. Biopsy reveals antigen-antibody complexes deposited in the kidney glomeruli. Which hypersensitivity type best explains this?
AType I — IgE bound to mast cells triggered histamine release in the kidney
BType II — IgG antibodies recognized and attacked antigens directly on glomerular basement membrane cells
CType III — soluble immune complexes deposited in the glomeruli and activated complement locally, causing tissue damage
DType IV — sensitized T cells infiltrated the kidney and caused direct cytotoxicity
Type III hypersensitivity is defined by immune complex deposition in tissues. When antigen-antibody complexes accumulate in the blood and deposit in vessel walls, kidneys, or joints, they activate complement locally, recruiting neutrophils that release enzymes causing tissue damage. Post-streptococcal glomerulonephritis is the textbook Type III example. Type II also involves antibodies but requires them to be directed against antigens ON the cell surface — not free circulating complexes.
Question 3 True / False
Type IV hypersensitivity, unlike Types I–III, can occur in the complete absence of antibodies.
TTrue
FFalse
Answer: True
Type IV is mediated entirely by T cells — sensitized CD4+ T helper cells that recruit macrophages, and CD8+ cytotoxic T cells that directly attack tissue. The tuberculin skin test and contact dermatitis are classic examples requiring no antibody at all. This is fundamentally different from Types I (IgE), II (IgG/IgM against cell surfaces), and III (immune complexes). The 24–72 hour delay reflects the time needed for T cell activation, proliferation, and migration — a cellular process, not an antibody-mediated one.
Question 4 True / False
The 48–72 hour delay in Type IV hypersensitivity occurs because it takes that long for the immune system to produce new antibodies against the antigen.
TTrue
FFalse
Answer: False
Type IV does not involve antibodies at all. The delay reflects the time required for memory T cells to recognize the antigen, become activated, proliferate, and migrate to the tissue site — an entirely cellular process. Types I–III can occur rapidly (especially Type I, within minutes) precisely because they rely on pre-existing antibodies or antibody-sensitized cells. Misattributing the Type IV delay to antibody production conflates T cell and B cell kinetics.
Question 5 Short Answer
Why does correctly identifying the type of hypersensitivity reaction matter for treatment selection?
Think about your answer, then reveal below.
Model answer: The four types involve fundamentally different immune effectors, so treatments targeting one mechanism have no effect on others. Antihistamines block histamine from mast cell degranulation in Type I but cannot help a Type IV reaction. Plasmapheresis removes circulating antibodies and complexes in Types II and III. Corticosteroids suppress T cell activity and macrophage recruitment in Type IV. Matching treatment to mechanism is essential because the effectors causing damage are completely different across types.
This is why the Gell and Coombs classification was developed — not as a taxonomic exercise but to enable rational, mechanism-based therapy. A clinician who misidentifies the mechanism will apply the wrong treatment, which at best does nothing and at worst exacerbates the condition by suppressing the wrong arm of the immune response.